Serum Level of Fibrinogen A.ALPHA. Chain Fragment Increases in Chronic Thromboembolic Pulmonary Hypertension

Yano, Toshiaki; Sogawa, Kazuyuki; Umemura, Hiroshi; Sakao, Seiichiro; Kasahara, Yasunori; Tanabe, Nobuhiro; Kodera, Yasuhiro; Takiguchi, Yuichi; Nomura, Fumio

doi:10.1253/circj.cj-11-0045

Cited by 8 publications

(4 citation statements)

References 35 publications

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“…Subsequently, several studies confirmed that increased plasma/serum levels of fibrinogen are detectable in CTEPH (and PH) patients as compared to unaffected controls [25,26], supporting the idea that fibrinogen from patients carrying the Aα Thr312Ala polymorphism (or other polymorphisms affecting the structure of fibrinogen) is indeed more resistant to lysis. Finally, in 2013, Li et al confirmed in a large study including 101 CTEPH, 102 PE (without PH), and 108 healthy controls a higher genotype and allele frequency for the Aα Thr312Ala polymorphism in CTEPH [27].…”

Section: Polymorphismsmentioning

confidence: 89%

Molecular Research in Chronic Thromboembolic Pulmonary Hypertension

Opitz

Kirschner

2019

IJMS

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Chronic Thromboembolic Pulmonary Hypertension (CTEPH) is a debilitating disease, for which the underlying pathophysiological mechanisms have yet to be fully elucidated. Occurrence of a pulmonary embolism (PE) is a major risk factor for the development of CTEPH, with non-resolution of the thrombus being considered the main cause of CTEPH. Polymorphisms in the α-chain of fibrinogen have been linked to resistance to fibrinolysis in CTEPH patients, and could be responsible for development and disease progression. However, it is likely that additional genetic predisposition, as well as genetic and molecular alterations occurring as a consequence of tissue remodeling in the pulmonary arteries following a persistent PE, also play an important role in CTEPH. This review summarises the current knowledge regarding genetic differences between CTEPH patients and controls (with or without pulmonary hypertension). Mutations in BMPR2, differential gene and microRNA expression, and the transcription factor FoxO1 have been suggested to be involved in the processes underlying the development of CTEPH. While these studies provide the first indications regarding important dysregulated pathways in CTEPH (e.g., TGF-β and PI3K signaling), additional in-depth investigations are required to fully understand the complex processes leading to CTEPH.

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Section: Polymorphismsmentioning

confidence: 89%

Molecular Research in Chronic Thromboembolic Pulmonary Hypertension

Opitz

Kirschner

2019

IJMS

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“…This study is notable for its incorporation of plasma protein depletion techniques, specifically albumin and immunoglobulin G. Despite immunodepletion of these two highly abundant proteins, penetration into the lower abundant proteome proved difficult. To overcome this dynamic range problem, Nomura and colleagues took advantage of a high‐throughput workflow that utilizes MALDI TOF/TOF MS of low molecular weight serum peptides from CTEPH patients. This technique employs magnetic beads with various surface chemistries in lieu of SELDI technology, and identified fibrinogen A alpha chain fragment as increased in CTEPH.…”

Section: Proteomics Has Already Catapulted Research In Phmentioning

confidence: 99%

Proteomics of pulmonary hypertension: Could personalized profiles lead to personalized medicine?

Colvin

Yeager

2015

Proteomics Clinical Apps

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Pulmonary hypertension (PH) is a fatal syndrome that arises from a multifactorial and complex background, is characterized by increased pulmonary vascular resistance and right heart afterload, and often leads to cor pulmonale. Over the past decades, remarkable progress has been made in reducing patient symptoms and delaying the progression of the disease. Unfortunately, PH remains a disease with no cure. The substantial heterogeneity of PH continues to be a major limitation to the development of newer and more efficacious therapies. New advances in our understanding of the biological pathways leading to such a complex pathogenesis will require the identification of the important proteins and protein networks that differ between a healthy lung (or right ventricle) and a remodeled lung in an individual with PH. In this article, we present the case for the increased use of proteomics-the study of proteins and protein networks-as a discovery tool for key proteins and protein networks operational in the PH lung. We review recent applications of proteomics in PH, and summarize the biological pathways identified. Finally, we attempt to presage what the future will bring with regard to proteomics in PH and offer our perspectives on the prospects of developing personalized proteomics and custom-tailored therapies.

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“…12 In proteomic analysis, serum levels of the fibrinogen Aα chain fragment were found to be higher in chronic thromboembolic pulmonary hypertension. 13 Therefore, the spectrum of CVD in which fibrinogen is emerging as either a marker of increased risk or a contributor to the pathogenesis is expanding. It has been proposed that the fibrinogen level may be included in the risk stratification of CVD.…”

Section: Fibrinogen: a Marker Of Risk For Cvdmentioning

confidence: 99%